Biomedical subjects
Publications and source records attributed to A C Kroes.
In a population-based case-control study of 474 patients with a first episode of deep-vein thrombosis and 474 age-matched and sex-matched controls, we found no effect of Chlamydia pneumoniae infection on the occurrence of deep-vein thrombosis.
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BACKGROUND: Cytomegalovirus disease is still a major problem in immunocompromised patients, such as bone marrow or kidney transplantation patients. The detection of viral antigen in leukocytes (antigenemia) has proven to be a clinically relevant marker of CMV activity and has found widespread application. Because most existing assays are rather time-consuming and laborious, an accelerated version (Brite Turbo) of an existing method (Brite) has been developed. The major modification is in the direct lysis of erythrocytes instead of separation by sedimentation. OBJECTIVE: In this study the Brite Turbo method has been compared with the conventional Brite method to detect CMV antigen pp65 in peripheral blood leukocytes of 107 consecutive immunocompromised patients. RESULTS: Both tests produced similar results. Discrepancies were limited to the lowest positive range and sensitivity and specificity were comparable for both tests. CONCLUSIONS: Two major advantages of the Brite Turbo method could be observed in comparison to the original method: assay-time was reduced by more than 50% and only 2 ml of blood was required. An additional advantage was the higher number of positive nuclei in the Brite Turbo method attributable to the increased number of granulocytes in the assay. Early detection of CMV infection or reactivation has become faster and easier with this modified assay.
BACKGROUND: To further improve the safety of the blood supply, various national blood transfusion organizations presently use or are in the process of implementing routine HCV NAT in minipools. According to the Committee for Proprietary Medicinal Products (CPMP) of the European Union, the HCV NAT detection limit of the assay should be 100 IU per mL (270 geq/mL) for testing initial plasma pools. Paul Ehrlich Institute (PEI) regulations stipulate that 5000 IU per mL (13,500 geq/mL) must be detected to calculate the amount contributed by individual donations composing the minipool. The sensitivity for HCV RNA extraction achieved by three commercially available laboratory kits was compared. STUDY DESIGN AND METHODS: Nucleic acids from 1-in-3 serial dilutions of an HCV RNA run control (Pelispy, CLB) were extracted with three kits (Cobas Amplicor, Roche Diagnostic Systems; BioRobot 9604, Qiagen; and NucliSens Extractor, Organon Teknika). HCV PCR of all extracts was performed using a second-generation Cobas Amplicor HCV test and the Cobas Amplicor analyzer. RESULTS: The manual Cobas Amplicor, the BioRobot 9604, and the NucliSens Extractor setups allow a 95-percent HCV RNA detection limit of 129, 82, and 12 geq per mL, respectively. The maximal pool size for the manual Cobas Amplicor, the BioRobot 9604, and the NucliSens Extractor kits that would still meet the PEI criteria for HCV NAT in minipools was calculated at 104, 164, and 1125 donations, respectively. CONCLUSION: All three HCV NAT kits evaluated meet the criteria set by CPMP and PEI. The highest sensitivity for HCV NAT screening can be achieved with the high-volume NucliSens Extractor method in combination with the Cobas Amplicor HCV v2.0 test on the Cobas Amplicor analyzer.
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Infection by the human parvovirus B19 can lead to several clinical manifestations which are relevant in internal medicine. These include aplastic crisis in chronic haemolytic anaemias, exanthemathous disease and arthropathy, mainly in women, and chronic anaemia in the immunocompromised host. After initial replication, probably in the respiratory tract, the virus enters its target cells in the bone marrow, erythroid precursor cells, through its receptor, the blood group P antigen. Viral replication in these cells leads to an arrest in erythropoiesis, normally lasting approximately 1 week. In this stage, an aplastic crisis can be produced in all patients under 'erythropoietic stress'. The viraemia disappears as specific antibodies to the virus become detectable in serum, which may give rise to a rash or arthralgia, symptoms that are probably immune-mediated. In immunologically normal individuals the infection is cleared by the humoral immune system within several weeks, whereafter detectable specific IgG confers lifelong immunity to reinfection. In patients with absent or dysfunctional humoral immunity to this virus, however, persistent infection can occur, which results in chronic suppression of erythropoiesis with chronic anaemia. Passive immunization, by means of normal immunoglobulin preparations has been reported to be effective in treating this condition. Diagnosis of parvovirus infection is usually possible by the detection of specific antibodies of IgM class in cases of recent infection. In patients with aplastic crisis and patients with chronic anaemia diagnosis rests upon the detection of parvovirus B19 DNA in serum by polymerase chain reaction. Parvovirus B19 is a ubiquitous virus. By the age of 15, about 50% of individuals have serologic evidence of a past infection, which may present as the common childhood disease erythema infectiosum. At the age of 70, seroprevalence reaches 80 to 100%. A vaccine against this virus is currently being developed.
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A detailed description is presented of the hemodialysis treatment for 6 weeks of a patient strongly positive for hepatitis B virus ([HBV], hepatitis B surface antigen, hepatitis B e antigen, HBV DNA), which was performed without any special precautions. All 59 patients potentially exposed to the HBV-positive patient, of whom 29 appeared fully unprotected by antibody, were followed for at least 9 months but remained negative. This illustrates the feasibility of following Universal Precautions instead of using exceptional procedures for one single agent.
Exhaled nitric oxide (NO) is elevated in asthmatics, and varies with disease severity. We postulated that a respiratory virus infection increases exhaled NO levels in asthma, and examined the relationship between the virus-induced changes in exhaled NO and in airway hyperresponsiveness to histamine. In a parallel study, seven patients underwent experimental rhinovirus 16 (RV16) inoculation at days 0 and 1, whilst seven patients received placebo. Exhaled NO was measured at baseline (day 0) and at days 1, 2 and 3 after inoculation. Histamine challenges were performed prior to (day -7) and after inoculation (day 3), and were expressed as provocative concentration causing a 20% fall in forced expiratory volume in one second (FEV1) (PC20). Following RV16 infection there was a significant increase in NO at days 2 and 3 as compared to baseline (median change (range): 4.2 (7.5) parts per billion (ppb), p=0.03, and 3.0 (10.1) ppb, p=0.02, respectively). Furthermore, PC20 decreased significantly following RV16 infection (mean+/-SD change in doubling dose: -0.65+/-0.54, p=0.02), whereas PC20 did not change in the placebo group (p=0.1). There was a significant correlation between the RV16-induced changes in exhaled NO levels at day 2 and the accompanying changes in PC20 at day 3 (rank correlation coefficient (rs): 0.86, p=0.01). Hence, the greater the increase in exhaled NO, the smaller the decrease in PC20. We conclude that rhinovirus infection increases exhaled nitric oxide levels in asthmatics, and that this increase is inversely associated with worsening of airway hyperresponsiveness to histamine. These results suggest that viral induction of nitric oxide synthase within the airways may play a protective role in exacerbations of asthma.
OBJECTIVE: To determine whether vaccination against hepatitis B may be omitted in persons with isolated positive anti-HBc. DESIGN: Prospective study using control groups. SETTING'S: Heeren Loo-Lozenoord, Ermelo, the Netherlands. METHOD: Twenty-six older residents (group P) with isolated anti-HBc positivity (HBsAg negative and anti-HBs < 10 IU/l) were given hepatitis B vaccine (3 doses); 16 matched controls (group C1) lacking hepatitis B markers, received a primary vaccination (3 doses), 8 controls (group C2) with a immune status based on infection in the past received vaccination (3 doses) and 27 controls (group C3) were given a booster vaccination (1 dose) after vaccination 7 years earlier. The anti-HBs response was measured 0, 1 and 7 months after the first vaccine dose. An anamnestic response was defined as a fourfold rise of anti-HBs after one dose of vaccine or--in the absence of an anti-HBs titer in the prevaccination serum--a response > or = 10 IU/l after one dose of vaccine. A primary response was defined as an anti-HBs response > or = 10 IU/l after giving 3 vaccines, while the criteria for an anamnestic response were not met. RESULTS: In the isolated anti-HBc group (P) and in the corresponding control group (C2) 15 and 12.5%, respectively, showed an anamnestic response; the majority reacted with a primary response or did not respond at all. The subjects given a primary vaccination (C1) responded in 62.5% with a primary response while those vaccinated earlier (C3) responded in 92.6% with a fourfold rise of anti-HBs. CONCLUSIONS: The anti-HBs response to vaccination in older mentally handicapped persons is delayed and there is a reduced chance of development of a protective anti-HBs titer. The majority of individuals with isolated anti-HBc showed a primary response. In these persons vaccination should not be omitted, especially if there is a risk of hepatitis B.
Generalized lymphoproliferative disease occurred in a 30-year-old woman 15 days after she underwent simultaneous pancreas-kidney transplantation. Because of the rapid progression of this disorder, it was necessary to remove the grafts and discontinue immunosuppression 19 days after transplantation. Serological analysis demonstrated that the patient, who was Epstein-Barr virus (EBV)-seronegative 3 months before, was seroconverting at the time of the transplantation. EBV therefore was acquired just before the transplantation, either by a blood transfusion 4 months earlier or from the patient's EBV-positive boyfriend. The latter source appeared most likely, as concluded from the investigation of the EBV strains from the patient's boyfriend and from the blood and organ donors. Donor origin of lymphoblastoid cells was excluded by sex chromosomal analysis. Initiation of immunosuppression during a primary EBV infection carries the risk of very rapid development of B-cell lymphoproliferative disease. This emphasizes the need for active monitoring of EBV infections in transplant recipients and for the development of preventive strategies.
Disturbance of the balance between excitatory and inhibitory activity of the airway sensory nerves has been implicated in asthma pathogenesis, particularly during exacerbations of the disease. The objective of this study was to examine the effect of experimental rhinovirus 16 (RV16) infection on airway responsiveness to bradykinin, a potent sensory nerve stimulus, in asthma. Thirteen atopic, mildly asthmatic subjects participated in a parallel, placebo-controlled study. A total dose of 2.6 to 5.6 x 10(4) TCID50 RV16 (n = 7) or its diluent (n = 6) was inoculated on 2 consecutive days (Days 0 and 1). Histamine and bradykinin challenges were performed before (Days-7 and-6) and after (Days 3 and 4) inoculation. The response was measured by FEV1 and partial flow-volume curves, and it was expressed as PC20FEV1 and PC40V40p, respectively (changes expressed in doubling dose: DD). Before inoculation, PC20FEV1 and PC40V40p to histamine were not significantly different between the groups (p > or = 0.22), whereas PC20FEV1 and PC40V40p to bradykinin tended to be higher in the RV16 group (p = 0.11 and p = 0.06, respectively). PC20FEV1 and PC40V40p to histamine decreased significantly in the RV16 group (mean change +/- SEM: -0.65 +/- 0.20 DD, p = 0.02 and -0.98 +/- 0.28 DD, p = 0.01, respectively), but not in the placebo group (p > or = 0.26). PC40V40p to bradykinin increased significantly in the placebo group (+2.46 +/- 0.92 DD, p = 0.04), with a similar trend for PC20FEV1 (+1.50 +/- 0.62 DD, p = 0.06), whereas there were no significant changes in the RV16 group (p > or = 0.77). These changes in PC40V40p to histamine and bradykinin were significantly different between the groups (p = 0.02). We conclude that repeated bradykinin challenge over a 10-d interval induces tachyphylaxis in asthmatic subjects in vivo and that experimental RV16 infection abolishes such tachyphylaxis to bradykinin while it enhances airway responsiveness to histamine. These results do not favor a predominant role of airway sensory nerves in rhinovirus-induced exacerbations of asthma.
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A man, 23 years of age, had a typical erythema infectiosum, complicated by a severe bilateral brachial plexus neuritis. Motor function recovered slowly and only partially after 6 months. An infection by human parvovirus B19 was demonstrated, with strongly positive and gradually declining IgM antibodies and viral DNA detectable in serum for more than 3 months. There was also clear evidence of a recent infection by cytomegalovirus. The interaction between these two viruses could be responsible for this rare and severe complication of common infections in this patient.
The potential association of human parvovirus B19 infection with idiopathic thrombocytopenic purpura (ITP) was studied. All 60 adult patients presenting with ITP at the University Hospital Rotterdam - Dijkzigt during a 12-year period (41 with acute ITP, 19 with chronic ITP) were included. Patient files were retrospectively analyzed. Stored serum samples were tested for parvovirus B19-specific IgG and IgM anti-bodies, and for parvovirus B19 DNA. In only one patient (1.7%) was evidence of recent B19 infection found. Parvovirus B19 is not a frequent cause of adult ITP and should be tested for only when there are other indications of possible parvovirus B19 involvement.
Parvovirus B19 infection may cause chronic anemia in human immunodeficiency virus (HIV)-infected hosts. Small-scale studies and case reports have suggested that parvovirus B19 infection is a significant cause of anemia in HIV-infected patients. We studied single serum samples from 317 consecutive HIV-infected patients with use of parvovirus B19-specific serology and polymerase chain reaction for detection of viral DNA. Anemia was noted in 176 patients (55.5%); 126 (39.9%) had < 0.10 x 10(9) CD4+ cells/L. In this study group, 191 (60.3%) of the patients were positive for parvovirus B19 IgG. Seroprevalence rates did not differ between patients with low and higher CD4+ cell counts or between anemic and nonanemic patients. Parvovirus B19 DNA was detected in none of the sera. In a control group of 226 healthy male blood donors, the seroprevalence of parvovirus B19 IgG was 68.1%; two IgG-positive sera also contained parvovirus B19 DNA. This study demonstrates that chronic parvovirus B19 infection should not be considered a frequent cause of anemia in HIV-infected individuals.
B cell lymphoproliferative disorders (BLPD) are relatively frequent after genotypically non-HLA-identical BMT. We performed univariate analysis to study which BMT-related variables were associated with an increased risk of developing BLPD. Sixty-five recipients of other than genotypically HLA-identical BM grafts were included in the study. Seventy-seven recipients of genotypically HLA-identical BM grafts served as a comparison group. BLPD occurred in nine of 65 children after non-HLA-identical BMT (14%) and in none of the 77 children after HLA-identical BMT (0%). In all cases, BLPD was proven to be EBV-related. Our data suggest that the combined use of Campath 1G and anti-LFA1 was associated with an increased risk of developing BLPD, particularly children who had received a T cell-depleted BM graft, using albumen density gradient sedimentation followed by E-rosetting, and who were conditioned with Ara-C, CY and TBL. In addition, T cell numbers below 50/microliters at 1 month and below 100/microliters at 2 months after BMT, respectively, were associated with an increased risk of developing BLPD. Longitudinal determination of T cell numbers after non-HLA-identical BMT is a simple method for identifying patients at risk of developing BLPD. In addition to monitoring levels of circulating EBV-infected lymphocytes, monitoring T cell numbers may allow early intervention to prevent progression of BLPD.